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June 11, 2018

Reisa Sperling, One of the world's foremost researchers of Alzheimer’s disease, was vacationing at Lake Tahoe with her family in 2008 when she noticed her father was behaving strangely.

“Where’s your mother?” he would ask, disoriented. “What are we doing here?”

At first, Sperling thought her dad, a 74-year-old chemistry professor, might simply be tired. Perhaps the altitude had affected him. And then she had a terrible thought: He was acting just like her grandfather — his own father — who had died of Alzheimer’s in 1993.

Yet a subsequent evaluation with his primary care doctor yielded a clean bill of health. The symptoms of forgetfulness seemed to dissipate. Sperling figured that, given her line of work, she had been overly vigilant. She did her best to quell those worries about her father.

About a year after the trip, she got interested in research that focused on a phase of Alzheimer’s that doctors knew little about: the preclinical phase. People in this stage still function normally, but unbeknownst to them, they already have buildup of a protein called amyloid — one of the two hallmark features of the disease — in their brains. (Alzheimer’s also involves abnormal tangles of another protein, tau, which emerge somewhat later in the disease process.) For the past 25 years, research has pivoted around the so-called amyloid hypothesis, which maintains that the buildup of amyloid plaques is the primary trigger for the mental deterioration wrought by the disease.

The preclinical phase, which can be identified by PET scans, typically lasts 10 or 15 years before significant memory problems set in.